硫普罗宁对阿霉素心脏毒性的保护作用及机制

目的：研究硫普罗宁（MPG）对阿霉素（ADM）心脏毒性的保护作用及机制。方法：建立ADM损伤大鼠心脏模型，灌胃给予MPG，检测血清肌钙蛋白Ⅰ（cTnⅠ）、肌酸激酶同工酶（CK-MB）及脑钠肽（BNP）、心肌组织超氧化物歧化酶（SOD）活力，丙二醛（MDA）、一氧化氮（NO）含量及一氧化氮合酶（NOS）的活性，并观察心肌组织病理改变。结果：与ADM大鼠心脏模型组相比，MPG干预ADM处理后大鼠的血清cTnⅠ、CK—MB及BNP显著降低（P〈0．05或P〈0．01），心肌组织SOD活力显著增高，MDA、NO含量，总NOS活力及iNOS活力显著降低（P均〈0．01），心肌组织病理积分显著下降（P〈0．05）。结论：MPG对ADM心脏毒性具有较好的保护作用；MPG可能通过恢复心肌组织SOD的活力、抑制iNOS活性使心肌组织NO产生减少，从而减轻ADM所致大鼠心肌组织的氧化损伤。

Study on protection and mechanism for adriamycin-induced cardiotoxicity with tiopronin in rats

AIM： To investigate the protection effect and mechanism of tiopronin on the cardiotoxicity induced by adriamycin in rats. METHODS： Rats were given intraperitoneal injection of adriamycin to induce the cardiotoxicity model. After continuous oral administration of tiopronin in adriamycin ＋ tiopronin gYoup for fourteen days, all the rats were killed. The content of cardiac troponin Ⅰ （cTn Ⅰ ）, MB isoenzyme of creatine kinase （CK-MB） and brain natriuretic peptide （BNP） in serum were monitored. The activities of superoxide dismutase（SOD）, the contents of malondialdehyde （MDA） and nitric oxide （NO）, the activities of nitric oxide synthase （NOS） in myocardial tissue were determined. Myocardial pathology changes of rat myocardium were detected. RESULTS： Comapared with adriamycin group, the content of cTn Ⅰ , CK-MB and BNP in serum were significantly decreased （P 〈0.05 or P 〈 0.01 ）, the activity of SOD in myocardial tissue was significantly increased, the contents of MDA and NO in myocardial tissue were significantly decreased, the activities of NOS and iNOS in myocardial tissue were significantly decreased（ P 〈 0.01 ）, the pathology integral was significantly decreased in adriamy- cin ＋ tiopronin group （ P 〈 0.05 ）. CONCLUSION： Tiopronin has a protective effect on adriamycin-induced cardiotoxicity in rats. Tiopronin could relieve the oxidative injury of myocardial tissue induced by adriamycin in rats by increasing the activity of SOD, inhibiting the activity of iNOS which decreases the contents of NO.